Acute Methanol Poisoning: Prevalence and Predisposing Factors of Haemorrhagic and Non‐Haemorrhagic Brain Lesions

Abstract

Abstract:The purpose was to study the prevalence and predisposing factors of brain lesions in survivors of acute methanol poisoning. Clinical data on 106 patients with methanol poisoning were collected during the Czech mass poisoning outbreak. Of 83 survivors, in 46 (55%) patients, follow-up examinations including magnetic resonance imaging of brain (MR) were performed 3-8 and 24-28 months after discharge from the hospital. Of 46 patients with a median age of 49 (interquartile range, 35-57) years, 24 (52%) patients had a total of 40 abnormal brain findings with haemorrhagic lesions detected in 15 (33%) and non-haemorrhagic lesions found in 9 (19%) patients. The patients with haemorrhagic brain lesions were more acidemic (lower arterial blood pH, higher base deficit) and had higher glycaemia and lactacidaemia on admission than those without haemorrhages (all p < 0.05). Thirteen of 32 (41%) of patients with systemic anticoagulation and 2 of 14 (14%) of patients without it had haemorrhagic lesions (p = 0.080). Bleeding complications during the treatment occurred in 4 of 15 (27%) patients, and 5 of 15 (33%) patients had conditions predisposing to haemorrhage in the group with haemorrhagic lesions. In three cases with a series of computer tomography (CT)/MR performed during hospitalization, the necrotic lesions in the brain remained non-haemorrhagic during hospitalization and haemorrhagic lesions were detected on the follow-up MR examinations only. No association between brain haemorrhages and systemic anticoagulation during dialysis was found: brain haemorrhages might occur in severely poisoned patients treated without systemic anticoagulation, whereas treatment with high doses of heparin might not lead to brain haemorrhages.Methanol poisoning due to the consumption of illicit alcoholic beverages represents an important medical problem throughout the world [1][2][3][4][5]. This poisoning generally occurs either intentionally through abuse or attempted suicide or unintentionally through misuse or accident [6,7]. Despite the progress in diagnosis and treatment of methanol poisoning, morbidity and mortality are still high [8,9]. If therapeutic measures are inadequate or delayed, mortality may exceed 40% and serious longterm visual and central nervous system (CNS) sequelae may occur [10][11][12]. The strategy of active case finding and prehospital ethanol administration in the patients with suspected poisoning can improve outcome in a large-scale outbreak of methanol poisoning [13,14].Methanol in the human organism is metabolized to the highly toxic formic acid/formate ion, which inhibits mitochondrial respiration [15][16][17][18]. The accumulation of formic acid results in metabolic acidosis, visual impairment and damage to basal ganglia [19][20][21]. Rapid administration of antidotes and haemodialysis are crucial for successful treatment [22][23][24][25]. Importance.The role of haemodialysis in the treatment of methanol poisoning is well-established: it effectively eliminates both methanol and formate and helps to cor...

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

“…In experimental TBI, the mechanical force can directly shear blood vessels and axons, damage neurons and glia, leading to intracerebral bleeding, brain tissue compression, lacerations, and contusions with quick activation of several biochemical cascades including neuroinflammation [46,47]. In non-traumatic brain damage caused by accumulating formic acid, the secondary effects evolve gradually through several stages during approximately 1 week after admission, as was demonstrated by the series of brain CT/MRI examinations during hospitalization in patients with acute methanol poisoning [9]. Our results correspond with the results of experimental studies demonstrating that neuroinflammatory responses persist for several weeks with zenith LT concentrations around day seven after brain injury [21,48,49].…”

“…Nevertheless, there is no difference in the serum formic acid concentrations in patients with lethal outcome and in survivors with sequelae of poisoning [17]. MRI signs of brain damage can be found in survivors of poisoning with low serum formic acid concentration on admission (2-4 mmol/L), while the patients with high serum formic acid concentration on admission of about 15 mmol/L may survive without CNS sequelae [9].…”

“…Bilateral necrosis of the basal ganglia and necrotic lesions in the subcortical white matter are typical magnetic resonance (MRI) signs of brain damage in acute methanol poisoning [7][8][9]. Methanol-induced optic neuropathy may resolve within a few weeks with complete recovery [10].…”

“…Brain lesions in patients with severe methanol poisoning pass through several stages during one to two weeks: general or multifocal subcortical white matter and pericapsular or focal basal ganglia edema followed by foci of non-hemorrhagic necrosis, which can progress to vast hemorrhagic necrotic lesions [9]. Formic acid in the brain possibly acts as a trigger initiating a complex array of pathologic and protective mechanisms including neuroinflammatory reaction mediated by LTs and the interaction of these mechanisms may determine the outcome of poisoning and the degree of brain and optic nerve damage in survivors.…”

Efficiency of acidemia correction on intermittent versus continuous hemodialysis in acute methanol poisoning

“…During an outbreak of methanol poisoning in the Czech Republic in 2012, [19][20][21][22][23][24][25][26][27][28][29] we compared the efficiency of ECTRs for correction of acidemia in relation to the severity of poisoning and burden of formate toxicity. The epidemiological description of the outbreak has been presented elsewhere.…”